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MRCP part 1 > Ophthalmology > Flashcards

Ophthalmology Flashcards

1
Q

what is dry macular degeneration characterised by?

A

• Dry macular degeneration: characterized by Drusen - yellow round spots in Bruch’s membrane

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2
Q

what is wet macular degeneration characterised by?

A

Wet (exudative, neovascular) macular degeneration: characterized by choroidal
neovascularisation. Leakage of serous fluid and blood can subsequently result in a rapid loss of vision. Carries worst prognosis

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3
Q

how is macular degeneration classified?

A

• Early age related macular degeneration (non-exudative, age related maculopathy): drusen and
alterations to the retinal pigment epithelium (RPE)
• Late age related macular degeneration (neovascularisation, exudative)

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4
Q

what are risk factors for macular degeneration?

A
  • Age: most patients are over 60 years of age
  • Family history
  • Smoking
  • More common in caucasians
  • ♀sex
  • High cumulative sunlight exposure
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5
Q

what are features of macular degeneration?

A
  • ↓ visual acuity: ‘blurred’, ‘distorted’ vision, central vision is affected first
  • Central scotomas
  • Fundoscopy: drusen, pigmentary changes
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6
Q

what is included in the general management of macular degeneration?

A

• Stopping smoking
• High does of β-carotene, vitamins C and E, and zinc may
help to slow down visual loss for patients with established macular degeneration. Should avoid smoking due to an ↑ risk of lung cancer

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7
Q

what is the management of wet macular degeneration?

A
  • Photocoagulation
  • Photodynamic therapy
  • anti-vascular endothelial growth factor (anti-VEGF) treatments: intravitreal ranibizumab
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8
Q

what are 5 causes of sudden painless loss of vision?

A
  • Ischemic optic neuropathy (e.g. Temporal arteritis or atherosclerosis)
  • Occlusion of central retinal vein
  • Occlusion of central retinal artery
  • Vitreous hemorrhage
  • Retinal detachment
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9
Q

describe the clinical features of amaurosis fugax?

A

Amaurosis fugax: classically described as a transient monocular vision loss that appears as a “curtain coming down vertically into the field of vision in one eye”. Sometimes it occurs as episodes, caused by ipsilateral carotid artery diease.

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10
Q

Ischaemic optic neuropathy:

  • what is this caused by?
  • what is the pathophysiology?
  • what visual defect is seen?
  • what is seen at fundoscopy?
A
  • May be due to arteritis (e.g. Temporal arteritis) or atherosclerosis (e.g. HTN, DM, old patient)
  • Due to occlusion of the short posterior ciliary arteries, causing damage to the optic nerve
  • Altitudinal field defects are seen → loss of vision above or below the horizontal level
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11
Q

Central retinal vein occlusion:

  • how does age affect incidence?
  • what are the causes?
  • what is seen at fundoscopy?
A
  • Incidence ↑ with age, more common than arterial occlusion
  • Causes: glaucoma, polycythemia, hypertension

Fundoscopy
• Widespread retinal haemorrhages in all 4 quadrants, which vary in appearance from a small-scattered retinal hemorrhages to marked confluent hemorrhages
• Marked dilated and tortuous retinal vessels
• Cotton-wool spots
• Optic disc edema, macular edema, and retinal
thickening
• Vitreous hemorrhages may be present

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12
Q

Central retinal artery occlusion:

  • causes
  • clinical features
  • fundoscopy findings
A
  • Due to thromboembolism (from atherosclerosis) or arteritis (e.g. Temporal arteritis)
  • Features include Afferent pupillary defect, ‘cherry red’ spot on a pale retina
  • Diffuse edema makes the retina and arteries look pale. Perfused underlying tissues show through the thin fovea giving a classic cherry-red spot appearance
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13
Q

Vitreous haemorrhage:

  • causes
  • features
  • points on history
A

• Causes: diabetes, bleeding disorders
• Features may include sudden visual loss,
dark spots
• Large bleeds cause sudden visual loss
• Moderate bleeds may be described as numerous dark spots
• Small bleeds may cause floaters

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14
Q

what are the clinical features seen in posterior vitreous detachment?

A
  • Flashes of light (photopsia) - in the peripheral field of vision
  • Floaters, often on the temporal side of the central vision
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15
Q

what clinical features are seen in retinal detachment?

A
  • Dense shadow that starts peripherally progresses towards the central vision
  • A veil or curtain over the field of vision
  • Straight lines appear curved (positive Amsler grid test)
  • Central visual loss
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16
Q

where is the lesion in a relative afferent pupillary defect?

A

Relative afferent pupillary defect: Also known as the Marcus-Gunn pupil, a relative afferent pupillary defect is found by the ‘swinging light test’. It is caused by a lesion anterior to the optic chiasm i.e. optic nerve or retina

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17
Q

what are two causes of RAPD?

A

Causes
• Retina: detachment
• Optic nerve: optic neuritis e.g. Multiple sclerosis

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18
Q

describe the afferent and efferent pathways of the pupillary light reflex

A

Pathway of pupillary light reflex
• Afferent: retina → optic nerve → lateral geniculate body → midbrain
• Efferent: edinger-westphal nucleus (midbrain) → oculomotor nerve

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19
Q
  • Third nerve palsy
  • Holmes-adie pupil
  • Traumatic iridoplegia
  • Pheochromocytoma
  • Congenital

All cause what kind of pupil?

A

mydriasis: large pupil

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20
Q

what are drug causes of mydriasis?

A

Drug causes of mydriasis
• Topical mydriatics: tropicamide, atropine
• Sympathomimetic drugs: amphetamines
• Anticholinergic drugs: tricyclic antidepressants

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21
Q

who is holmes-adie pupil seen in? what kind of pupil is seen?

A

Holmes-ADIe pupil is a benign condition most commonly seen in women. It is one of the differentials of a DIlated pupil

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22
Q

Holmes-adie pupil:

  • is this bilateral or unilateral?
  • what happens once the pupil has constricted?
  • is this reactive to accomodation? to light?
A

• Unilateral in 80% of cases
• Dilated pupil
• Once the pupil has constricted it remains small for an
abnormally long time
• Slowly reactive to accommodation but very poorly (if at all) to light

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23
Q

The absence of which reflexes are associated with holmes adie pupil - called holmes adie syndrome?

A

Holmes-Adie syndrome

• Association of Holmes-Adie pupil with absent ankle/knee reflexes

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24
Q

what is angioid retinal streaks on fundoscopy?

A

Angioid retinal streaks are seen on fundoscopy as irregular dark red streaks radiating from
the optic nerve head. The elastic layer of Bruch’s membrane is characteristically thickened and calcified

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25
Q
  • Pseudoxanthoma elasticum
  • Ehler-danlos syndrome
  • Paget’s disease
  • Sickle-cell anemia
  • Acromegaly

can all cause?

A

angioid retinal streaks

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26
Q

what is optic atrophy?

A

Optic atrophy is seen as pale, well demarcated disc on fundoscopy. It is usually bilateral and causes a gradual loss of vision. Causes may be acquired or congenital

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27
Q
  • Multiple sclerosis
  • papilledema (longstanding)
  • raised intraocular pressure (e.g. glaucoma, tumour)
  • retinal damage (e.g. choroiditis, retinitis pigmentosa)
  • ischemia
  • toxins: tobacco amblyopia, quinine, methanol, arsenic, lead
  • nutritional: vitamin B1, B2, B6 and B12 deficiency

are all acquired causes of?

A

optic atrophy

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28
Q

• Friedreich’s ataxia
• Mitochondrial disorders e.g. Leber’s optic atrophy
• DIDMOAD - the association of cranial Diabetes Insipidus,
Diabetes Mellitus, Optic Atrophy and Deafness (also known as Wolfram’s syndrome)

are all congenital causes of?

A

optic atrophy

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29
Q

what are systemic causes for cataract?

A 
• DM
• Steroids
• Infection (congenital rubella)
• Metabolic (hypocalcemia,
galactosemia)
• Myotonic dystrophy, Down's
syndrome
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30
Q

what are ocular causes for cataract?

A
  • Trauma
  • Uveitis
  • High myopia
  • Topical steroids
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31
Q

what are the clinical features of retinitis pigmentosa?

A

Retinitis pigmentosa primarily affects the peripheral retina resulting in tunnel vision

Features
• Night blindness is often the initial sign
• Funnel vision (the preferred term for tunnel vision)

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32
Q 
• Refsum disease: cerebellar ataxia, peripheral
neuropathy, deafness, ichthyosis
• Usher syndrome
• Abetalipoproteinemia
• Lawrence-Moon-Biedl syndrome
• Kearns-Sayre syndrome
• Alport's syndrome

are all disease assoc with?

A

retinitis pigmentosa

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33
Q

what is seen at fundoscopy of retinitis pigmentosa?

A

Mottling of the retinal pigment epithelium with black bone-spicule pigmentation is typically indicative (or pathognomonic) of retinitis pigmentosa. Other ocular features include waxy pallor of the optic nerve head, attenuation (thinning) of the retinal vessels, cellophane maculopathy, cystic macular edema and posterior subcapsular cataract

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34
Q

what does CMV retinitis cause?

A

CMV Retinitis: causes hemorrhage at the edge of the area of retinal necrosis

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35
Q

list causes for funnel vision

A
  • Papilledema • Retinitis pigmentosa
  • Glaucoma • Choroidoretinitis
  • Optic atrophy secondary to tabes dorsalis
  • Hysteria
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36
Q

describe typical Congenital Hypertrophy of the Retinal Pigment Epithelium (CHRPE)

A

Typical CHRPE:
• Gray or black depigmented lacunae
• Found in 1 quadrant of eye
• Do not affect vision

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37
Q

describe atypical Congenital Hypertrophy of the Retinal Pigment Epithelium (CHRPE)
-what investigation should be done?

A

Atypical CHRPE:
• White fish tail shaped bilaterally
• Affect the vision when there are > 4 in each eye
• Associated with Adenosis polyposis and Gardner’s syndrome → do colonoscopy.

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38
Q

what is glaucoma?

A

Glaucoma is a group disorders characterized by optic neuropathy due, in the majority of patients, to raised intraocular pressure (IOP). It is now recognised that a minority of patients with raised IOP do not have glaucoma and vice versa

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39
Q

what is acute angle glaucoma?

  • what is this rise in IOP secondary to?
  • what factors predispose to acute angle glaucoma?
A

In acute angle closure glaucoma (AACG) there is a rise in IOP secondary to an impairment of aqueous outflow. Factors predisposing to AACG include:
• Hypermetropia (long-sightedness)
• Pupillary dilatation
• Lens growth associated with age

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40
Q

what drugs may precipitate acute angle glaucoma?

A

Mydriatic drops are a known precipitant of acute angle closure glaucoma. Drugs which may precipitate acute glaucoma include anticholinergics and tricyclic antidepressants.

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41
Q

what are the clinical features of acute angle glaucoma?

A
  • Severe pain: may be ocular or headache
  • ↓ visual acuity
  • Symptoms worse with mydriasis (e.g. Watching TV in a dark room)
  • Hard, red eye
  • Haloes around lights
  • Semi-dilated non-reacting pupil
  • Corneal edema results in dull or hazy cornea
  • Systemic upset may be seen, such as nausea and vomiting and even abdominal pain
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42
Q

what is the management of acute angle glaucoma?

A

Management
• Urgent referral to an ophthalmologist
• Management options include reducing aqueous secretion with acetazolamide and pupillary
constriction with topical pilocarpine

Treatment of acute glaucoma - acetazolamide + pilocarpine

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43
Q

what are the risk factors for primary open-angle glaucoma?

A 
Primary open-angle glaucoma (POAG) also referred to as chronic simple glaucoma: it is present in around 2% of people older than 40 years. Other than age, risk factors include:
• Family history
• Black patients • Myopia
• Hypertension
• Diabetes mellitus
44
Q

which type of glaucoma is assoc with either hypermetropia or myopia?

A

Acute angle closure glaucoma is associated with hypermetropia Primary open-angle glaucoma is associated with myopia

45
Q

what are the features of primary open angle glaucoma?

A

POAG may present insidiously and for this reason is often detected during routine optometry appointments. Features may include:
• Peripheral visual field loss - nasal scotomas progressing to ‘tunnel vision’
• ↓ visual acuity
• Optic disc cupping

46
Q

Prostaglandin analogues:

  • give an example
  • how do these work?
  • how are these administrated?
  • what are the adverse effects?
A

Prostaglandin analogues (e.g. Latanoprost)

  • ↑ uveoscleral outflow
  • Once daily administration
  • Adverse effects include brown pigmentation of the iris
47
Q

β-blocker

  • give an example
  • how do these work?
  • what are the adverse effects?
A

β-blockers (e.g. Timolol)

  • ↓ aqueous production
  • Should be avoided in asthmatics and patients with heart block
48
Q

Sympathomimetics:

  • give an example
  • how do these work?
  • when to avoid?
  • what are the adverse effects?
A

Sympathomimetics (e.g. Brimonidine, an α2-adrenoceptor agonist)

  • ↓ aqueous production and ↑ outflow
  • Avoid if taking MAOI or tricyclic antidepressants
  • Adverse effects include hyperemia
49
Q

Carbonic anhydrase inhibitors:

  • give an example
  • how do these work?
  • what are the adverse effects?
A

Carbonic anhydrase inhibitors (e.g. Dorzolamide)

  • ↓ aqueous production
  • Systemic absorption may cause sulphonamide-like reactions
50
Q

Miotics:

  • give an example
  • how do these work?
  • what are the adverse effects?
A

Miotics (e.g. Pilocarpine)

  • ↑ uveoscleral outflow
  • Adverse effects included a constricted pupil, headache and blurred vision
51
Q

what may be considered it treatment refractory glaucoma?

A

Surgery in the form of a trabeculectomy may be considered in refractory cases.

52
Q

Red eye with: small, fixed oval pupil, ciliary flush

A

• Uveitis: small, fixed oval pupil, ciliary flush

53
Q

Red eye with: severe pain, haloes, ‘semi-dilated’ pupil

A

• Glaucoma: severe pain, haloes, ‘semi-dilated’ pupil

54
Q 
• Severe pain (may be ocular or headache)
• ↓ visual acuity, patient sees haloes
• Semi-dilated pupil
• Hazy cornea
disease?
A

Acute angle glaucoma

55
Q

• Severe pain (may be worse on movement) and tenderness
• May be underlying autoimmune disease e.g. Rheumatoid arthritis
disease?

A

scleritis

56
Q

• Acute onset • Pain
• Blurred vision and photophobia
• Small, fixed oval pupil, ciliary flush
disease?

A

anterior uveitis

57
Q

• Purulent discharge if bacterial, clear discharge if viral

disease?

A

conjunctivitis

58
Q

Red eye with History of trauma or coughing bouts

A

subconjunctival haemorrhage

59
Q

what is dacryocysitis?

-what are the features?

A

Dacryocystitis is infection of the lacrimal sac, Features:
• Watering eye (epiphora)
• Swelling and erythema at the inner canthus of the eye

60
Q

what is the management of dacryocystitis?

A

Management is with systemic antibiotics. (IV antibiotics are indicated if there is associated periorbital cellulitis)

61
Q

what is blepharitis and what is this due to?

A

Blepharitis is inflammation of the eyelid margins. It may due to meibomian gland dysfunction (common, posterior blepharitis) or seborrhoeic dermatitis/staphylococcal infection (less common, anterior blepharitis). Blepharitis is also more common in patients with rosacea

62
Q

what do the meibomian glands do?

A

The meibomian glands secrete oil on to the eye surface to prevent rapid evaporation of the tear film. Any problem affecting the meibomian glands (as in blepharitis) can hence cause drying of the eyes which in turns leads to irritation

63
Q

what are the clinical features of blepharitis?

A

Features
• Symptoms are usually bilateral
• Grittiness and discomfort, particularly around the eyelid margins
• Eyes may be sticky in the morning
• Eyelid margins may be red. Swollen eyelids may be seen in staphylococcal blepharitis
• Styes and chalazions are more common in patients with blepharitis
• Secondary conjunctivitis may occur

64
Q

what is the management of blepharitis?

A

Management
• Softening of the lid margin using hot compresses twice a day
• Mechanical removal of the debris from lid margins - cotton wool buds dipped in a mixture of
cooled boiled water and baby shampoo/sodium bicarb in recently boiled water is often used
• Artificial tears may be given for symptom relief in people with dry eyes or an abnormal tear film

65
Q

what are 5 ocular manifestations of rheumatoid arthritis?

A
  • Keratoconjunctivitis sicca (most common)
  • Episcleritis (erythema)
  • Scleritis (erythema and pain)
  • Corneal ulceration
  • Keratitis → associated with acns rosacea
66
Q

how to differentiate scleritis from episcleritis?

A

Scleritis is painful, episcleritis is not painful

67
Q

what are iatrogenic manifestations of eye disease?

A

Iatrogenic
• Steroid-induced cataracts
• Chloroquine retinopathy

68
Q

Thyroid eye disease:

  • how many people does this affect?
  • what is this due to?
  • will the patient be eu- hypo- or hyper- thyroid at presentation?
A

Thyroid eye disease affects between 25-50% of patients with Graves’ disease. It is thought to be due to an autoimmune response against an autoantigen, possibly the TSH receptor, causing retro- orbital inflammation. The patient may be eu-, hypo- or hyperthyroid at the time of presentation

69
Q

what is involved in the prevention of thyroid eye disease?

A
  • Smoking is the most important modifiable risk factor for the development of thyroid eye disease
  • Radioiodine treatment may ↑ the inflammatory symptoms seen in thyroid eye disease. In a recent study of patients with Graves’ disease around 15% developed, or had worsening of, eye disease. Prednisolone may help ↓ the risk
70
Q

what are the clinical features of thyroid eye disease?

A
  • Exophthalmos
  • Conjunctival edema
  • Papilledema
  • Ophthalmoplegia
  • Inability to close the eye lids may lead to sore, dry eyes. If severe and untreated patients can be at risk of exposure keratopathy
71
Q

what is the management of thyroid eye disease?

A
  • Topical lubricants may be needed to help prevent corneal inflammation caused by exposure
  • Steroids
  • Radiotherapy
  • Surgery
72
Q

what is herpes zoster ophthalmicus?

A

Herpes Zoster Ophthalmicus (HZO) describes the reactivation of the varicella zoster virus in the area supplied by the ophthalmic division of the trigeminal nerve. It accounts for around 10% of case of shingles.

73
Q

what are the features of herpes zoster ophthalmicus?

A

• Vesicular rash around the eye, which may or may not involve the actual eye itself
• Hutchinson’s sign: rash on the tip or side of the nose. Indicates nasociliary involvement and is a
strong risk factor for ocular involvement

74
Q

what is the management of herpes zoster ophthalmicus?

A
  • Oral antiviral treatment for 7-10 days ideally started within 72 hours. Topical antiviral treatment is not given in HZO
  • Oral corticosteroids may reduce the duration of pain but do not reduce the incidence of post- herpetic neuralgia
  • Ocular involvement requires urgent ophthalmology review
75
Q

what are the complications of herpes zoster ophthalmicus?

A
  • Ocular: conjunctivitis, keratitis, episcleritis, anterior uveitis
  • Ptosis
  • Post-herpetic neuralgia
76
Q

how does herpes simplex keratitis most commonly present?

A

Herpes Simplex Keratitis most commonly presents with a dendritic corneal ulcer

77
Q

what are the clinical features of herpes simplex keratitis?

A 
• Red, painful eye
• Photophobia
• Epiphora
• Visual acuity may be ↓
• Fluorescein staining may show an epithelial ulcer, dendritic
pattern of staining.
78
Q

what is the management of herpes simplex keratitis?

A

Management
• Immediate referral to an ophthalmologist
• Topical acyclovir

79
Q

what is band keratopathy?

A

Band keratopathy: is a corneal disease derived from the appearance of calcium on the central cornea caused by calcium deposition in Bowman’s layer. This is an example of metastatic calcification, which by definition, occurs in the presence of hypercalcemia

80
Q

what are the symptoms of band keratopathy?

A

Symptoms include pain and decreased visual acuity.

81
Q

what is the treatment of band keratopathy?

A

Treatment: the calcium can be scraped off the cornea or removed with a laser. This can restore sight, but it can take a number of months for normal vision to return as the cornea will be damaged during the operation. This cannot be repeated too many times as it would make the cornea thinner and thinner.

82
Q

describe the pathophysiology of diabetic retinopathy?

A

Diabetic Retinopathy is the most common cause of blindness in adults aged 35-65 years-old. Hyperglycemia is thought to cause ↑ retinal blood flow and abnormal metabolism in the retinal vessel walls. This precipitates damage to endothelial cells and pericytes.
Endothelial dysfunction leads to ↑ vascular permeability which causes the characteristic exudates seen on fundoscopy. Pericyte dysfunction predisposes to the formation of microaneurysms. Neovasculization is thought to be caused by the production of growth factors in response to retinal ischemia

83
Q

describe the prevalence of macular edema

A
  • 2-6% of background retinopathy
  • 20-60%preproliferative retinopathy
  • 70-75% of proliferative cases.
84
Q

what are the risk factors for macular oedema?

A
  • ↑ HbA1c
  • Protienuria
  • Duration of DM
85
Q

the traditional classification of diabetic retinopathy was background retinopathy and pre-proliferative retinopathy.
describe background retinopathy

A

Background retinopathy
• Microaneurysms (dots)
• Blots hemorrhages (=3)
• Hard exudates

86
Q

the traditional classification of diabetic retinopathy was background retinopathy and pre-proliferative retinopathy.
describe pre-proliferative retinopathy

A
  • Cotton wool spots (soft exudates; ischemic nerve fibres)
  • > 3 blots hemorrhages
  • V enous beading/looping
  • Deep/dark cluster hemorrhages
  • More common in type I DM, treat with laser photocoagulation
87
Q

The new classification of diabetic retinopathy is mild, moderate and severe non-proliferative diabetic retinopathy (NPDR) and proliferative retinopathy.
Describe mild NPDR

A

• 1 or more microaneurysm

88
Q

The new classification of diabetic retinopathy is mild, moderate and severe non-proliferative diabetic retinopathy (NPDR) and proliferative retinopathy.
Describe moderate NPDR

A

• Microaneurysms
• Blot hemorrhages
• Hard exudates
• Cotton wool spots, venous beading/looping and
intraretinal microvascular abnormalities (IRMA) less severe than in severe NPDR

89
Q

The new classification of diabetic retinopathy is mild, moderate and severe non-proliferative diabetic retinopathy (NPDR) and proliferative retinopathy.
Describe severe NPDR

A

• Blot hemorrhages and microaneurysms in 4
quadrants
• Venous beading in at least 2 quadrants
• IRMA in at least 1 quadrant

90
Q

The new classification of diabetic retinopathy is mild, moderate and severe non-proliferative diabetic retinopathy (NPDR) and proliferative retinopathy.
Describe proliferative retinopathy.
- what is the management

A

Proliferative retinopathy → (urgent referral to an ophthalmologist for panretinal photocoagulation)
• Retinal neovascularisation - may lead to vitrous hemorrhage
• Fibrous tissue forming anterior to retinal disc
• More common in type I DM, 50% blind in 5 years

91
Q

what is the earliest sign of proliferative retinopathy?

A

Microaneurysm on fluorescein angiography is the earlist sign of DM Nephropathy

92
Q

what is diabetic maculopathy?

A

Maculopathy
• Based on location rather than severity, anything is potentially serious
• Hard exudates and other ‘background’ changes on macula
• Check visual acuity
• More common in type II DM

93
Q

Asymmetric DM Retinopathy → suspect ?

A

Asymmetric DM Retinopathy → suspect ocular ischemia (carotid artery disease)

94
Q

describe the diabetic retinopathy screening for T1DM?

A

• T1DM
o Newly diagnosed DM → after 5 years
o From 5-10 years → anuual
o More than 10 years DM → 6 monthly

95
Q

describe the diabetic retinopathy screening for T2DM?

A

• T2DM

o Anually

96
Q

what are 3 causes of optic neuritis?

A
  • Multiple sclerosis
  • Diabetes
  • Syphilis
97
Q

what are the features of optic neuritis?

A
  • Unilateral ↓ in visual acuity over hours or days
  • Poor discrimination of colors, ‘red desaturation’
  • Pain worse on eye movement
  • Relative afferent pupillary defect
  • Central scotoma
98
Q

What guides prognosis in optic neuritis?

A

Prognosis

• MRI: if > 3 white-matter lesions, 5-year risk of developing multiple sclerosis is c. 50%

99
Q

what is retrobulbar neuritis?

A

Retrobulbar Neuritis: inflammation behind the optic nerve head, the optic disc is normal.

100
Q

what are the features of retrobulbar neuritis?

A

Features:
• Visual acuity loss
• Afferent pupillary defect during swinging flashing light
• Color vision will be reduced (red looks pallor)

101
Q

describe what a trochlear nerve palsy causes

A

Trochlear Nerve Palsy: cause torsional diplopia, Torsion is a normal response to tilting the head sideways. The eyes automatically rotate in an equal and opposite direction, so that the orientation of the environment remains unchanged – vertical things remain vertical.

102
Q

Describe Keith-Wagener classification of hypertensive retinopathy stage I

A

Arteriolar narrowing and tortuosity

Increased light reflex - silver wiring

103
Q

Describe Keith-Wagener classification of hypertensive retinopathy stage II

A

Arteriovenous nipping

104
Q

Describe Keith-Wagener classification of hypertensive retinopathy stage III

A

Cotton-wool exudates

Flame and blot haemorrhages

105
Q

Describe Keith-Wagener classification of hypertensive retinopathy stage IV

A

Papilloedema

106
Q

what are the 1st, 2nd and 3rd line drugs in glaucoma?

A

first line: prostaglandin analogue (PGA) eyedrop
second line: beta-blocker, carbonic anhydrase inhibitor, or sympathomimetic eyedrop
if more advanced: surgery or laser treatment can be tried2

MRCP part 1 (17 decks)

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